Short-term plasticity shapes activity pattern-dependent striato-pallidal synaptic transmission

The cortico-striato (Str)-globus pallidus external segment (GPe) projection plays major roles in the control of neuronal activity in the basal ganglia under both normal and pathological conditions. The present study used rat brain-slice preparations to address our hypothesis that the gain of this disynaptic projection is dynamically controlled by activations of short-term plasticity mechanisms of Str-GPe synapses. The Str-GPe projection neurons fire with very different frequency and firing patterns in vivo depending on the condition of the animal. The results show that the Str-GPe synapses have very strong short-term enhancement mechanisms and that repetitive burst activation of the Str-GPe synapses, which mimic oscillatory burst firing of Str neurons, can sustain enhanced states of synaptic transmission for tens of seconds. The results reveal that the short-term enhancement of Str-GPe synapses contributes to the generation of pauses in the firing of GPe neurons and that signal transfer function in the Str-GPe projection is highly dependent on the firing pattern of Str neurons.

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Short-Term Plasticity Turns Plastic. Focus on “Synaptic Transmission at the Calyx of Held Under In Vivo-Like Activity Levels”

Journal of Neurophysiology ◽

10.1152/jn.00641.2007 ◽

2007 ◽

Vol 98 (2) ◽

pp. 577-578 ◽

Cited By ~ 2

Author(s):

Erwin Neher

Keyword(s):

Synaptic Transmission ◽

Activity Levels ◽

Short Term ◽

Calyx Of Held ◽

Short Term Plasticity

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Disruption of Cholinergic Circuits as an Area for Targeted Drug Treatment of Alzheimer’s Disease: In Vivo Assessment of Short-Term Plasticity in Rat Brain

Pharmaceuticals ◽

10.3390/ph13100297 ◽

2020 ◽

Vol 13 (10) ◽

pp. 297

Author(s):

Vergine Chavushyan ◽

Ani Soghomonyan ◽

Gohar Karapetyan ◽

Karen Simonyan ◽

Konstantin Yenkoyan

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Synaptic Transmission ◽

Rat Brain ◽

Basolateral Amygdala ◽

Neural Circuits ◽

Short Term ◽

Short Term Plasticity ◽

Excitatory Responses

The search for new therapeutics for the treatment of Alzheimer’s disease (AD) is still in progress. Aberrant pathways of synaptic transmission in basal forebrain cholinergic neural circuits are thought to be associated with the progression of AD. However, the effect of amyloid-beta (Aβ) on short-term plasticity (STP) of cholinergic circuits in the nucleus basalis magnocellularis (NBM) is largely unknown. STP assessment in rat brain cholinergic circuitry may indicate a new target for AD cholinergic therapeutics. Thus, we aimed to study in vivo electrophysiological patterns of synaptic activity in NBM-hippocampus and NBM-basolateral amygdala circuits associated with AD-like neurodegeneration. The extracellular single-unit recordings of responses from the hippocampal and basolateral amygdala neurons to high-frequency stimulation (HFS) of the NBM were performed after intracerebroventricular injection of Aβ 25–35. We found that after Aβ 25–35 exposure the number of hippocampal neurons exhibiting inhibitory responses to HFS of NBM is decreased. The reverse tendency was seen in the basolateral amygdala inhibitory neural populations, whereas the number of amygdala neurons with excitatory responses decreased. The low intensity of inhibitory and excitatory responses during HFS and post-stimulus period is probably due to the anomalous basal synaptic transmission and excitability of hippocampal and amygdala neurons. These functional changes were accompanied by structural alteration of hippocampal, amygdala, and NBM neurons. We have thus demonstrated that Aβ 25–35 induces STP disruption in NBM-hippocampus and NBM-basolateral amygdala circuits as manifested by unbalanced excitatory/inhibitory responses and their frequency. The results of this study may contribute to a better understanding of synaptic integrity. We believe that advancing our understanding of in vivo mechanisms of synaptic plasticity disruption in specific neural circuits could lead to effective drug searches for AD treatment.

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Frequency-Dependent Modulation of Short-Term Plasticity of GABAergic Synaptic Transmission

International Journal of Physiology and Pathophysiology ◽

10.1615/intjphyspathophys.v9.i2.30 ◽

2018 ◽

Vol 9 (2) ◽

pp. 119-126

Author(s):

Oksana P. Kolesnyk ◽

Svetlana A. Fedulova ◽

Mycola S. Veselovsky

Keyword(s):

Synaptic Transmission ◽

Short Term ◽

Frequency Dependent ◽

Short Term Plasticity ◽

Gabaergic Synaptic Transmission

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Nitric oxide-soluble guanylyl cyclase signaling regulates corticostriatal transmission and short-term synaptic plasticity of striatal projection neurons recorded in vivo

Neuropharmacology ◽

10.1016/j.neuropharm.2009.11.011 ◽

2010 ◽

Vol 58 (3) ◽

pp. 624-631 ◽

Cited By ~ 27

Author(s):

Stephen Sammut ◽

Sarah Threlfell ◽

Anthony R. West

Keyword(s):

Nitric Oxide ◽

Synaptic Plasticity ◽

Guanylyl Cyclase ◽

Soluble Guanylyl Cyclase ◽

Projection Neurons ◽

Short Term ◽

Striatal Projection Neurons

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Short-Term Plasticity at Inhibitory Synapses in Rat Striatum and Its Effects on Striatal Output

Journal of Neurophysiology ◽

10.1152/jn.2001.85.5.2088 ◽

2001 ◽

Vol 85 (5) ◽

pp. 2088-2099 ◽

Cited By ~ 25

Author(s):

John S. Fitzpatrick ◽

Garnik Akopian ◽

John P. Walsh

Keyword(s):

Action Potentials ◽

Brain Slices ◽

Current Injection ◽

Inhibitory Synapses ◽

Rat Striatum ◽

Short Term ◽

Short Term Plasticity ◽

Adult Rat ◽

Glutamate Receptor Antagonists

Two forms of short-term plasticity at inhibitory synapses were investigated in adult rat striatal brain slices using intracellular recordings. Intrastriatal stimulation in the presence of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (20 μM) andd,l-2-amino-5-phosphonovaleric acid (50 μM) produced an inhibitory postsynaptic potential (IPSP) that reversed polarity at −76 ± 1 (SE) mV and was sensitive to bicuculline (30 μM). The IPSP rectified at hyperpolarized membrane potentials due in part to activation of K+ channels. The IPSP exhibited two forms of short-term plasticity, paired-pulse depression (PPD) and synaptic augmentation. PPD lasted for several seconds and was greatest at interstimulus intervals (ISIs) of several hundred milliseconds, reducing the IPSP to 80 ± 2% of its control amplitude at an ISI of 200 ms. Augmentation of the IPSP, elicited by a conditioning train of 15 stimuli applied at 20 Hz, was 119 ± 1% of control when sampled 2 s after the conditioning train. Augmentation decayed with a time constant of 10 s. We tested if PPD and augmentation modify the ability of the IPSP to prevent the generation of action potentials. A train of action potentials triggered by a depolarizing current injection of constant amplitude could be interrupted by stimulation of an IPSP. If this IPSP was the second in a pair of IPSPs, it was less effective in blocking spikes due to PPD. By contrast, augmented IPSPs were more effective in blocking spikes. The same results were achieved when action potentials were triggered by a depolarizing current injection of varying amplitude, a manipulation that produces nearly identical spike times from trial to trial and approximates the in vivo behavior of these neurons. These results demonstrate that short-term plasticity of inhibition can modify the output of the striatum and thus may be an important component of information processing during behaviors that involve the striatum.

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Muscarinic presynaptic modulation in GABAergic pallidal synapses of the rat

Journal of Neurophysiology ◽

10.1152/jn.00385.2014 ◽

2015 ◽

Vol 113 (3) ◽

pp. 796-807 ◽

Cited By ~ 7

Author(s):

Ricardo Hernández-Martínez ◽

José J. Aceves ◽

Pavel E. Rueda-Orozco ◽

Teresa Hernández-Flores ◽

Omar Hernández-González ◽

...

Keyword(s):

Receptor Agonist ◽

Projection Neurons ◽

Quantal Content ◽

Short Term ◽

Paired Pulse ◽

Short Term Plasticity ◽

Striatal Projection Neurons ◽

Muscarinic Cholinergic ◽

Muscarinic Modulation

The external globus pallidus (GPe) is central for basal ganglia processing. It expresses muscarinic cholinergic receptors and receives cholinergic afferents from the pedunculopontine nuclei (PPN) and other regions. The role of these receptors and afferents is unknown. Muscarinic M1-type receptors are expressed by synapses from striatal projection neurons (SPNs). Because axons from SPNs project to the GPe, one hypothesis is that striatopallidal GABAergic terminals may be modulated by M1 receptors. Alternatively, some M1 receptors may be postsynaptic in some pallidal neurons. Evidence of muscarinic modulation in any of these elements would suggest that cholinergic afferents from the PPN, or other sources, could modulate the function of the GPe. In this study, we show this evidence using striatopallidal slice preparations: after field stimulation in the striatum, the cholinergic muscarinic receptor agonist muscarine significantly reduced the amplitude of inhibitory postsynaptic currents (IPSCs) from synapses that exhibited short-term synaptic facilitation. This inhibition was associated with significant increases in paired-pulse facilitation, and quantal content was proportional to IPSC amplitude. These actions were blocked by atropine, pirenzepine, and mamba toxin-7, suggesting that receptors involved were M1. In addition, we found that some pallidal neurons have functional postsynaptic M1 receptors. Moreover, some evoked IPSCs exhibited short-term depression and a different kind of modulation: they were indirectly modulated by muscarine via the activation of presynaptic cannabinoid CB1 receptors. Thus pallidal synapses presenting distinct forms of short-term plasticity were modulated differently.

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A General Model of Synaptic Transmission and Short-Term Plasticity

Neuron ◽

10.1016/j.neuron.2009.03.025 ◽

2009 ◽

Vol 62 (4) ◽

pp. 539-554 ◽

Cited By ~ 105

Author(s):

Bin Pan ◽

Robert S. Zucker

Keyword(s):

Synaptic Transmission ◽

General Model ◽

Short Term ◽

Short Term Plasticity

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Acute hypoxia induces elevation of ornithine decarboxylase activity in neonatal rat brain slices

Reproduction Fertility and Development ◽

10.1071/rd9950385 ◽

1995 ◽

Vol 7 (3) ◽

pp. 385 ◽

Cited By ~ 2

Author(s):

LD Longo ◽

S Packianathan

Keyword(s):

Rat Brain ◽

Ornithine Decarboxylase ◽

Bovine Serum ◽

Brain Slice ◽

Brain Slices ◽

Neonatal Rat ◽

Newborn Rat ◽

Rat Brain Slice

Recent studies in vivo have demonstrated that ornithine decarboxylase (ODC) activity in the fetal rat brain is elevated 4-5-fold by acute maternal hypoxia. This hypoxic-associated increase is seen in the rat brain in both the newborn and the adult. Because of the intimate involvement of ODC in transcription and translation, as well as in growth and development, it is imperative that the manner in which hypoxia affects the regulation of this enzyme be better understood. In order to achieve this, a brain preparation in vitro was required to eliminate the confounding effects of the dam on the fetal and newborn brain ODC activity in vivo. Therefore, brain slices from 3-4-day-old (P-3) newborn rats were utilized to test the hypothesis that ODC activity increases in response to hypoxia in vitro. Cerebral slices from the P-3 rat pups were allowed to equilibrate and recover in artificial cerebrospinal fluid (ACSF) continuously bubbled with a mixture of 95% O2 and 5% CO2 for 1 h before beginning hypoxic exposures. Higher basal ODC activities were obtained by treating the slices with 0.03% fetal bovine serum (FBS) and 0.003% bovine serum albumin (BSA), rather than with ACSF alone. Hypoxia was induced in the slices by replacing the gas with 40%, 21%, 10%, or 5% O2, all with 5% CO2 and balance N2. With FBS and BSA treatment, ODC activity was maintained at about 0.15-0.11 nM CO2 mg-1 protein h-1 throughout the experiment, which was 2-3-fold higher than that without FBS and BSA. ODC activity increased significantly and peaked between 1 h and 2 h after initiation of hypoxia. For instance, with 21% O2, ODC activity increased approximately 1.5-fold at 1 h and approximately 2-fold at 2 h. These studies demonstrate that: (1) the hypoxic-induced increases observed in vivo in the fetal and newborn rat brain ODC activity can be approximated in a newborn rat brain slice preparation in vitro; (2) newborn rat brain slice preparations may provide an alternative to methods in vivo or cell culture methods for studying the regulation of acute hypoxic-induced enzymes; and (3) high, stable baseline ODC activities in brain slices suggest that the cells in the slice are capable of active metabolism if FBS and BSA are available to mimic conditions in vivo.

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